Abstract

[Author Affiliation]Sara Anne Haack. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington.Paul R. Borghesani. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington.Aaron J. Green. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington.John F. Neumaier. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington.Stanley I. Shyn. Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington.Address correspondence to: Stanley I. Shyn, MD, PhD, Box 359911, Harborview Medical Center, Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98104, E-mail: stanshyn@uw.eduTo The Editor:Catatonia was first described in 1874 by Karl Kahlbaum, and in the American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 5th ed. (DSM-5) is a specifier (not an independent disorder) requiring 3 of 12 possible symptoms, including: Stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, odd mannerisms, stereotypies, agitation, grimacing, echolalia, and echopraxia (American Psychiatric Association 2013). Historically linked with schizophrenia, catatonia can also present in other mental disorders, as a result of other medical issues, and drugs. Notably, in situations where there is another mental disorder, as many as two thirds of patients with catatonia meet criteria for a mood disorder, often bipolar disorder (Weder et al. 2008).Benzodiazepines are first-line treatments for catatonia, and lorazepam response is often considered diagnostically corroborative. Still, only 70% of cases remit with benzodiazepines (Hawkins et al. 1995), and a variety of treatments are now used as adjuncts, including amantadine (Northoff et al. 1997; Hervey et al. 2012), memantine (Thomas et al. 2005; Obregon et al. 2011), and zolpidem (Thomas et al. 1997). In refractory cases, the use of electroconvulsive therapy (ECT) is supported by a limited case literature, with initial remission rates of 75% and sustained recovery at 6 months in 46% of pediatric catatonia cases (Rey and Walter 1997).In this report, we discuss a young patient admitted to our care following a 1.5-year-long course, whose catatonia responded well to ECT but who, nevertheless, continued to present diagnostic and management challenges.Case ReportJ., an 18-year-old Caucasian male, was transferred to our facility to initiate ECT for catatonia following two outside hospitalizations during the previous 5 weeks. On admission, J. was bedridden and on tube feeds, with stupor, waxy flexibility, mutism, negativism, and posturing. Prior to this, he had undergone extensive evaluation that included brain MRIs, electroencephalogram (EEG), lumbar puncture, a paraneoplastic antibody panel, transthoracic echocardiogram, and serologies for HIV, Herpes simplex virus (HSV), Toxoplasma gondii, Cryptococcus, and West Nile virus. None of these studies were revealing.Prior to age 17, J. had had an unremarkable history. He first became symptomatic his junior year in high school, when he began having more difficulty making decisions, and withdrew socially. After treatment-emergent anxiety and suicidality on paroxetine, and with positive depressive scores on two mood scales, bipolar disorder became the leading diagnosis. To target bipolar depression, olanzapine, ziprasidone, venlafaxine, sertraline, and quetiapine were successively trialed in outpatient care, but with prohibitive side effects or nonresponse.J.'s difficulties continued with a romantic breakup and plummeting grades. He mentioned, My body doesn't feel right. By spring of his senior year, J. exhibited compulsions, for example, repeatedly exiting and re-entering cars. Soon his deterioration became so severe that he stopped attending school. …

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